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Opening of the conference. From left to right: A. Belotserkovsky (Chairman of the Program Committee), A. Tuzikov (Chairman of PRIP-2021), S. Ablameyko (Deputy Chairman of PRIP-2021), S. Gaponenko (Chairman of the Belarusian Republican Foundation for Fundamental Research).
PMC9258759
11493_2022_6228_Fig1_HTML.jpg
0.457908
6fa0c0a4274a4713bc2312c99203d7bb
Schematic diagram of complex network relationship in the innovation community.
PMC9259225
JEPH2022-7359420.001.jpg
0.502988
21a46481714149f5bd3e42e3e9d8e10f
Classification of mainstream community networks.
PMC9259225
JEPH2022-7359420.002.jpg
0.426592
72bd904e8c414481a3e8f87ec986bb33
Research progress in an innovative community environment.
PMC9259225
JEPH2022-7359420.003.jpg
0.48565
e8a8500d45b94c6abd3ab9c986029756
Fission form of community communication.
PMC9259225
JEPH2022-7359420.004.jpg
0.431104
9765c03081d54c88b8b50a00f1e72f67
Top 10 players in Tiktok county.
PMC9259225
JEPH2022-7359420.005.jpg
0.422133
8ac7e27c43d24b64969adeceef602ceb
Sigmar1 deletion has no influence on bone mass under steady conditions AMicrocomputed tomography (micro‐CT) images of the proximal femur from 12‐week‐old male WT and Sigmar1 gKO mice. Scale bars, 1 mm.BQuantification of bone volume per tissue volume (BV/TV), trabecular number (Tb. N), trabecular separation (Tb. Sp), trabecular thickness (Tb. Th), cortical region BV/TV (Ct. BV/TV), and cortical thickness (Ct. Th, mm) (n = 5 biological replicates).CCoronal images of the fifth lumbar spine. Scale bars, 1 mm.DQuantification of trabecular bone parameters of lumbar spine (n = 5 biological replicates).ETRAP staining of tibias from male WT and Sigmar1 gKO mice. Scale bars, 50 μm.F, GQuantification of osteoclast number per bone surface (N. Oc/BS) and percentage of osteoclast surface per bone surface (Oc. S/BS) (n = 6 biological replicates).H, IRepresentative images and quantitative analysis of calcein double labeling. Scale bars, 20 μm (n = 6 biological replicates).J, KSerum PINP (procollagen I N‐terminal propeptide) and CTX‐I (C‐terminal telopeptide of type I collagen) concentrations measured by ELISA in male Sigmar1 gKO mice and their WT littermates (n = 6 biological replicates).LMSCs from male WT or Sigmar1 gKO mice underwent osteogenic differentiation for 7 or 21 days and staining for alkaline phosphatase or alizarin red, respectively. Data information: All results are representative data generated from at least three independent experiments. Data are presented as mean ± SD. The unpaired two‐tailed Student’s t‐test (B, D, F, G, I, J, and K) was used for statistical analysis.
PMC9260208
EMMM-14-e15373-g002.jpg
0.405882
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Dimemorfan alleviates joint destruction and osteoclast activity in CIA mice AThe schematic illustrates the protocol for CIA induction and dimemorfan treatment.BPhotographs of representative gross lesions in the hind limbs of CIA mice for clinical assessment.C, DArthritis in PBS‐treated and dimemorfan‐treated mice was induced by chicken type II collagen injection (n = 6 mice per group and per time point). After the second immunization, the arthritis score (C) and hind paw thickness (D) were evaluated every 5 days.EMicro‐CT images of paws from CIA mice with different treatments. Scale bars, 2 mm.FH&E staining of ankle joints from the three groups. Scale bars, 50 μm.GCell infiltrate (left), synovial hyperplasia (middle), and bone/cartilage erosion (right) of sections from different groups were analyzed (n = 5 biological replicates).HTRAP staining of ankle joints from the three groups. Scale bars, 50 μm.IThe number of TRAP‐positive cells per field of tissue sections stained with TRAP at 100× magnification was analyzed (n = 6 biological replicates).J–LSerum IL‐1β, IL‐6, and TNF‐α concentrations measured by ELISA in three groups (n = 5 biological replicates). Data information: All results are representative data generated from at least three independent experiments. Data are presented as mean ± SD. The one‐way ANOVA with the Tukey’s multiple comparison test (D and I–L) and nonparameter test (C and G) were used for statistical analysis. **P < 0.01. ***P < 0.001 versus PBS group.
PMC9260208
EMMM-14-e15373-g003.jpg
0.41529
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Sigmar1 deletion results in severe osteoporosis in the OVX model and promotes osteoclastogenesis in vitro AMicro‐CT images of the proximal femur from female WT or Sigmar1 gKO mice that received sham or ovariectomy surgery for 6 weeks. Scale bars, 1 mm.BQuantification of bone volume per tissue volume (BV/TV), trabecular number (Tb. N), trabecular separation (Tb. Sp), and trabecular thickness (Tb. Th) (n = 5 biological replicates).CTRAP staining of femur sections from the four groups. Scale bars, 200 μm.D, EQuantification of osteoclast number per bone surface (N. Oc/BS) and percentage of osteoclast surface per bone surface (Oc. S/BS) (n = 5 biological replicates).FTRAP staining to detect osteoclastogenesis of BMMs from WT or Sigmar1 gKO mice. Scale bars, 200 μm.G, HQuantification of the size and nuclei numbers of TRAP‐positive multinuclear cells (n = 6 biological replicates for G and n = 3 biological replicates for H).I, JRepresentative images and quantification of the relative pit resorption area of hydroxyapatite‐coated plates. WT or Sigmar1 gKO BMMs were seeded on hydroxyapatite‐coated plates and treated with 50 ng/ml RANKL (n = 6 biological replicates). Data information: All results are representative data generated from at least three independent experiments. Data are presented as mean ± SD. The one‐way ANOVA with the Tukey’s multiple comparison test (B, D, and E) and unpaired two‐tailed Student’s t‐test (G, H, and J) were used for statistical analysis.
PMC9260208
EMMM-14-e15373-g004.jpg
0.395655
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Sigmar1 interacts with SERCA2 and mediates its degradation Relative xbp1 splicing level of WT or Sigmar1 gKO BMMs during osteoclast formation measured by RT‐qPCR (n = 6 biological replicates).Immunoprecipitation of flag‐Sigmar1 interacting protein was visualized by silver gel staining.Western blots showing relative SERCA2 expression in WT and Sigmar1 gKO BMMs.Western blots showing truncated SERCA2 (314–807 aa) expression in HEK‐293T cells transfected with different amounts of Sigmar1 plasmids. The cells were transfected with 1 μg truncated SERCA2 plasmid and Sigmar1 plasmid (0.125, 0.25, 0.5, and 1 μg).Sequence alignment of glutamine residues from SERCA2 orthologs of different species.Western blots showing Q615A mutant full‐length SERCA2 expression in HEK‐293T cells in with different amounts of Sigmar1 plasmids. The cells were transfected with 1 μg Q615A mutant full‐length SERCA2 plasmid and Sigmar1 plasmid (0.125, 0.25, 0.5, and 1 μg).Interactions between Sigmar1 and WT or Q615 mutants of full‐length SERCA2 were detected by Co‐IP assays.Relative mRNA expression of SERCA2 in BMMs treated with PBS or 10 μM dimemorfan for 2 days (n = 6 biological replicates).Western blots showing SERCA2 expression in BMMs treated with PBS or 10 μM dimemorfan for 2 days.Relative SERCA2 activity in BMMs treated with PBS or dimemorfan was detected by the Ca2+‐ATPase assay (n = 6 biological replicates).Knock down of SERCA2 by siRNA in BMMs was verified by western blotting. Data information: All results are representative data generated from at least three independent experiments. Data are presented as mean ± SD. The unpaired two‐tailed Student’s t‐test (A, H and J) was used for statistical analysis. Source data are available online for this figure.
PMC9260208
EMMM-14-e15373-g005.jpg
0.424722
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Overexpression of Sigmar1 rescues OVX‐induced bone loss ASchematic illustrating the protocol for OVX‐induced bone loss and AAV‐Sigmar1 treatment. Briefly, 12‐week‐old mice were subjected to either sham or ovariectomy surgery together with different AAV intramedullary injection, and radiological analysis was conducted 6 weeks later.BMicro‐CT images of the proximal femur from sham or OVX mice with different AAV injections. Scale bars, 1 mm.CQuantification of bone volume per tissue volume (BV/TV), trabecular number (Tb. N), trabecular separation (Tb. Sp), and trabecular thickness (Tb. Th) (n = 5 biological replicates).DTRAP staining of femur sections from the three groups. Scale bars, 200 μm.E, FQuantification of osteoclast number per bone surface (N. Oc/BS) and percentage of osteoclast surface per bone surface (Oc. S/BS) (n = 5 biological replicates).GTRAP staining to detect osteoclastogenesis of BMMs treated with different Sigmar1 agonists (10 μM) or vector. Scale bars, 200 μm.H, IQuantification of the size and nuclei numbers of TRAP‐positive multinuclear cells (n = 6 biological replicates for H and n = 3 biological replicates for I).JWT MSCs underwent osteogenic differentiation for 7 or 21 days in the presence or absence of dimemorfan and was stained for alkaline phosphatase or alizarin red, respectively. Data information: All results are representative data generated from at least three independent experiments. Data are presented as mean ± SD. The one‐way ANOVA with the Tukey’s multiple comparison test (C, E, F, I, and K–O) was used for statistical analysis.
PMC9260208
EMMM-14-e15373-g007.jpg
0.415079
bd53ba5771f54c348857bb8cf2db46d7
Dimemorfan inhibits osteoclast differentiation in hPBMCs TRAP staining of hPBMCs treated with human RANKL (50 ng/ml) or dimemorfan for 12 days. Scale bars, 500 μm.Western blot analysis of NFATc1 expression during a 7‐day induction of hPBMCs to osteoclasts.hPBMCs were induced to differentiate into osteoclasts for 7 days, and the relative mRNA levels of marker genes were evaluated by RT‐qPCR (n = 6 biological replicates). Data information: All results are representative data generated from at least three independent experiments. Data are presented as mean ± SD. The one‐way ANOVA with the Tukey’s multiple comparison test (C) was used for statistical analysis. Source data are available online for this figure.
PMC9260208
EMMM-14-e15373-g008.jpg
0.500883
72090c7356cf499ab955c23780aedd44
Sigmar1 mediates SERCA2 degradation through the Hrd1/Sel1L‐dependent ERAD pathway A, BWestern blots showing SERCA2 expression in HEK‐293T cells with or without Sigmar1 co‐transfection treated with NMS‐873 or chloroquine at the indicated concentration. All inhibitors were applied to cells 8 h prior to protein collection.CWestern blots showing SERCA2 expression in BMMs treated with dimemorfan or vehicle for 48 h. Eeyarestatin I was added 8 h prior to cell harvest at indicated concentration.DHEK‐293T cells were transfected with different truncated SERCA2 lysine mutants and Sigmar1 and then subjected to western blot analysis.ESequence alignment of Ub sites in SERCA2 orthologs of different species. Data information: All results are representative data generated from at least three independent experiments. Source data are available online for this figure.
PMC9260208
EMMM-14-e15373-g009.jpg
0.423456
00986a083b4f4d8fb1b0a6c8d1fc64a1
Dimemorfan protects mice from established bone loss in various pathological models ASchematic illustrating the protocol for LPS‐induced osteolysis and dimemorfan treatment.BMicro‐CT images of calvaria from mice that received sham or LPS injection with PBS or dimemorfan treatment. Scale bars, 1 mm.CQuantification of bone volume/tissue volume (BV/TV) of calvaria from different groups (n = 6 biological replicates).DH&E and TRAP staining of calvaria from the three groups. Scale bars, 100 μm.E, FQuantification of osteoclast number per bone surface (N. Oc/BS) and percentage of osteoclast surface per bone surface (Oc. S/BS) (n = 6 biological replicates).GThe schematic illustrates the protocol for OVX‐induced bone loss and dimemorfan treatment.HMicro‐CT images of proximal femurs from sham or ovariectomized mice with different treatments. Scale bars, 1 mm.IQuantification of bone volume/tissue volume (BV/TV), trabecular number (Tb. N), trabecular separation (Tb. Sp), and trabecular thickness (Tb. Th) (n = 6 biological replicates).JTRAP staining of femurs from the three groups. Scale bars, 200 μm.K, LQuantification of osteoclast number per bone surface (N. Oc/BS) and percentage of osteoclast surface per bone surface (Oc. S/BS) (n = 6 biological replicates).M–OSerum IL‐1β, IL‐6, and TNF‐α concentrations measured by ELISA in the three groups (n = 5 biological replicates). Data information: All results are representative data generated from at least three independent experiments. Data are presented as mean ± SD. The one‐way ANOVA with the Tukey’s multiple comparison test (C, E‐F, I, and K–O) was used for statistical analysis.
PMC9260208
EMMM-14-e15373-g010.jpg
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Sigmar1 interacts with SERCA2 and mediates its degradation SERCA2 peptides identified through mass spectrometry are shown.HEK‐293T cells were transfected with the indicated plasmids and then subjected to immunoprecipitation followed by western blotting to detect exogenous interactions between Sigmar1 and SERCA2.The lysates from mouse BMMs were incubated with either anti‐Sigmar1 antibody or normal rabbit IgG, and the pellets were detected with the indicated antibodies.Western blots showing SERCA2 expression in HEK‐293T cells transfected with different amounts of Sigmar1 plasmids. The cells were transfected with 1 μg SERCA2 plasmid and Sigmar1 plasmid (0.125 μg, 0.25 μg, 0.5 μg, and 1 μg).Upper: schematic representation of various Sigmar1 truncations. Bottom: mapping of Sigmar1 domains critical for SERCA2 binding. HEK‐293T cells were transfected with different Sigmar1 truncations, and cell lysates were immunoprecipitated and subjected to western blotting.Upper: schematic representation of various SERCA2 truncations. Bottom: mapping of SERCA2 domains crucial for Sigmar1 binding. Different truncated SERCA2 plasmids were transfected into HEK‐293T cells. After immunoprecipitation, the interaction between truncated SERCA2 and Sigmar1 was detected by western blotting. Red asterisks indicate specific SERCA2 truncation bands.Binding mode of SERCA2 (positions 314–807) on the SIGMAR1 homotrimer predicted by docking. Upper: overall structure of SERCA2 bound to SIGMAR1 in cartoon view. SERCA2 and SIGMAR1 are colored in wheat and light blue, respectively, and the chain identifiers of the SIGMAR1 homotrimer are labeled. Middle and bottom: detailed interaction network between SERCA2 and SIGMAR1. Key residues of SERCA2 (deep teal) and SIGMAR1 (pink) are displayed as sticks, and chain identifiers of residues are shown. H‐bonds are displayed in red dashed lines, and the distances (acceptor to donor heavy atom) of H‐bonds are labeled.Western blots showing Q615A mutant‐truncated SERCA2 expression in HEK‐293T cells transfected with different amounts of Sigmar1 plasmids. The cells were transfected with 1 μg Q615A mutant of truncated SERCA2 plasmid and Sigmar1 plasmid (0.125, 0.25, 0.5, and 1 μg).Interactions between Sigmar1 and WT or Q615 mutants of truncated SERCA2 were detected by Co‐IP assays.TRAP staining to detect osteoclastogenesis of BMMs from WT and gKO mice treated with different siRNAs. Scale bars, 200 μm. Data information: All results are representative data generated from at least three independent experiments. Source data are available online for this figure.
PMC9260208
EMMM-14-e15373-g011.jpg
0.494628
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Sigmar1 deletion results in severe osteoporosis in the OVX model and promotes osteoclastogenesis in vitro AUterus weight from different groups (n = 6 biological replicates).BCoronal images of the fifth lumbar spine. Scale bars, 1 mm.CQuantification of trabecular bone parameters of lumbar spine (n = 5 biological replicates).D, EImmunohistochemistry staining of osteocalcin (Ocn) in femur sections (D) and quantification of Ocn‐positive osteoblast on trabecular bone surface (E) (n = 5 biological replicates). Data information: All results are representative data generated from at least three independent experiments. Data are presented as mean ± SD. The one‐way ANOVA with the Tukey’s multiple comparison test (A, C, and E) was used for statistical analysis. Source data are available online for this figure.
PMC9260208
EMMM-14-e15373-g012.jpg
0.47349
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Bone marrow transfer of Sigmar1 gKO cells exacerbates OVX‐induced osteoporosis AThe schematic illustrates the protocol for bone marrow transfer experiment and OVX surgery.BPCR bands for identifying success transfer of WT and Sigmar1 gKO bone marrow cells. Sigmar1 gKO cells had negative wt bands (upper), and positive mut bands (lower) and WT cells had the opposite results.CMicro‐CT images of the proximal femur from female ovariectomized mice that transferred with WT or Sigmar1 gKO bone marrow cells previously. Scale bars, 1 mm.DQuantification of bone volume per tissue volume (BV/TV), trabecular number (Tb. N), trabecular separation (Tb. Sp), and trabecular thickness (Tb. Th) (n = 8 biological replicates).EH&E staining of femur sections. Scale bars, 200 μm.FTRAP staining of femur sections. Scale bars, 200 μm.G, HQuantification of osteoclast number per bone surface (N. Oc/BS) and percentage of osteoclast surface per bone surface (Oc. S/BS) (n = 8 biological replicates). Data information: All results are representative data generated from at least three independent experiments. Data are presented as mean ± SD. Unpaired two‐tailed Student’s t‐test (D and G and H) was used for statistical analysis.
PMC9260208
EMMM-14-e15373-g013.jpg
0.510158
2245283a3178482a8a282a96f0658a17
Sigmar1 mediates SERCA2 degradation through the Hrd1/Sel1L‐dependent ERAD pathway A, BWestern blots showing SERCA2 expression in HEK‐293T cells with or without Sigmar1 co‐transfection treated with eeyarestatin I or MG‐132 at the indicated concentration. All inhibitors were applied to cells 8 h prior to protein collection.CWestern blots showing changes in SERCA2 expression in HEK‐293T cells in the presence of different doses of flag‐tagged Hrd1 plasmids.DWestern blots showing alterations of SERCA2 expression in HEK‐293T cells pretreated with negative control siRNA (si‐NC) or Sel1L siRNA in the presence or absence of Sigmar1.ETruncated myc‐tagged SERCA2 ubiquitination levels in HEK‐293T cells transfected with empty vector or Sigmar1 were analyzed by immunoprecipitation. Cells were treated with MG‐132 (10 μM) 8 h before harvest.FExpression of different truncated SERCA2 lysine mutants in HEK‐293T cells transfected with different amounts of Sigmar1 plasmid.GExpression of WT or 2KR (K460A and K541A) mutants of full‐length SERCA2 in HEK‐293T cells transfected with different amounts of Sigmar1 plasmid. Data information: All results are representative data generated from at least three independent experiments. Source data are available online for this figure.
PMC9260208
EMMM-14-e15373-g014.jpg
0.453623
6f02f68a38454c73ac632a5ce81eec3a
Representative HPV L1L2 VLP. A) Coomassie Blue stained SDS-PAGE depicting molecular weight marker, titration of bovine serum albumin as quantitative standards and a typical HPV L1L2 VLP sample including majority L1 capsid protein, minority L2 capsid protein and contaminating histones, likely encapsidated within the L1L2 VLP during maturation. ImageJ software used to estimate L1 concentration from BSA standards (National Institutes of Health, USA); B) negative stained electron microscopic image of HPV L1L2 VLP (Mag. 30,000x; JEM1400 high contrast Transmission Electron Microscope). C) Cross-binding checkerboard of mouse (M) immune sera raised against indicated L1L2 VLP (left column, including pre-immune pool, MPIP) and target L1L2 VLP antigen using Goat anti-Mouse IgG (H+L) biotinylated secondary antibody with the Median fluorescence intensities (MFI) of multiple (n = 4) coupling panels reported.
PMC9260319
gr1.jpg
0.457575
61ae5b09f00e435aaafde67b25172406
Frequency distribution plot of antibody levels including cumulative frequency plot (green line) derived from a panel of ‘likely negative’ serum samples against antigens in the 9-valent HPV L1L2 VLP Serology Assay. These data represent the pooled data for all sera against all antigens, but individual type-specific profiles are similar. BIN range represents the interval range (0.2 Units/mL) by which the data are categorized.
PMC9260319
gr2.jpg
0.427504
360918abc0ba4066b56eaf1154c251b6
Individual level specificity based upon the ‘false positive’ rate using the indicated algorithm and data from the ‘likely negative’ serum panel (n = 146). Impact assessment conducted using natural infection and vaccinee sera (n = 108) and associated agreement and Kappa statistics are shown. LOD, limit of detection.
PMC9260319
gr3.jpg
0.394514
b3fa58140a5f454d9b7fec3273424d8e
Sensitivity analysis to estimate the type-specific serostatus of indicated serum panels. The HPV Negative serum panel (n = 146) is the panel of ‘likely negative’ samples used to determine the LODs, while the Natural Infection (n = 201), Bivalent Vaccine (n = 27) and Quadrivalent Vaccine (n = 29) panels are used to compare the seroprevalence estimates resulting from application of the indicated algorithm to determine the LOD.
PMC9260319
gr4.jpg
0.4796
467c673469ba49a7b22599fe3652ec37
(A) Correlation between antibody levels (Log10 Units/mL) derived from the initial and repeat tests of vaccine and natural infection sera (n = 141) and (B) Compatibility between pseudovirion-based neutralization assay data and 9-valent binding data reported in IU/mL.
PMC9260319
gr5.jpg
0.569471
e4274ba55df5450da2a597bd30eb7484
Expression of rBbAMA-1(I/II) analyzed using SDS-PAGE stained with Coomassie brilliant blue (A) and western blotting analysis (B). Lane 1: Non-induced E. coli strain M15 containing pQE-32/BbAMA-1(I/II) plasmid; Lane 2: Induced E. coli strain M15 containing pQE-32/BbAMA-1(I/II) plasmid; Lane 3: Purified rBbAMA-1(I/II) protein. Black arrows indicate the target protein band of rBAMA-1(I/II).
PMC9260583
fvets-09-917389-g0001.jpg
0.454159
42578ddec5014953bb2479a6a397809f
Determination of rBbAMA-1(I/II)-specific antibody response. (A) Western blotting analysis demonstrated that pooled cattle serum immunized with rBbAMA-1(I/II) reacted with the purified recombinant protein (lane 1) when compared to the pre-immunization period (lane 2). (B) Indirect ELISA test revealed that the antibody response continuously increased after the first immunization with rBbAMA-1(I/II).
PMC9260583
fvets-09-917389-g0002.jpg
0.48398
7b29f15f85b94de8a0fd9af054233ab3
Time course of IgG2/IgG1 ratio response to rBbAMA-1(I/II) assessed by indirect ELISA. Each time point depicts the group mean value ± SD of the IgG2/IgG1 ratio. Asterisks indicate a significant difference (P < 0.05).
PMC9260583
fvets-09-917389-g0003.jpg
0.486565
3ec51f17b7714d46b637fef1822e4182
Determination of cellular immune response of cattle immunized with rBbAMA-1(I/II) analyzed by flow cytometry analysis. (A) Frequency of IFN-γ and TNF-α secreting CD4+ T cells. (B) Frequency of IFN-γ and TNF-α secreting CD8+ T cells. The results are expressed as group mean values ± SD. Asterisks indicate a significant difference (* < 0.05; *** < 0.001; **** < 0.0001). Experimental groups G1 = non-immunization, G2 = Montanide ISA 206 VG + PBS, G3 = rBbAMA-1(I/II) 50 μg + Montanide ISA 206 VG and G4 = rBbAMA-1(I/II) 100 μg + Montanide ISA 206 VG.
PMC9260583
fvets-09-917389-g0004.jpg
0.447183
94d469d4019545dfb4bcccb19fb42c01
Inflammatory cytokine gene expression profiles induced by rBbAMA-1(I/II). The results are expressed as mean values ± SD. Asterisks indicate a significant difference (* < 0.05; ** < 0.01; *** < 0.001). Experimental groups G1 = non-immunization, G2 = Montanide ISA 206 VG + PBS, G3 = rBbAMA-1(I/II) 50 μg + Montanide ISA 206 VG and G4 = rBbAMA-1(I/II) 100 μg + Montanide ISA 206 VG.
PMC9260583
fvets-09-917389-g0005.jpg
0.518301
2f980022eab54afdaa3dafc9936e500f
Summary of RNA-seq data. (A) Mapping rate of RNA-seq data of chloroplast (Chl) and mitochondria (Mito). (B) Codon position of RNA editing sites in two genotypes (CD, Caidao and WD, WD20342) of rice, chloroplast (Chl) genome, and mitochondrion (Mito) genomes. (C) Comparison of single nucleotide conversion in control and treated samples by RNA-seq approach. Values are shown by percentage. Number of total RES and edited genes. (D) Editing efficiency of all the RNA sites in rice chloroplast and mitochondrion genomes. For comparison, t-test was used. ***p < 0.001; **p < 0.01; *p < 0.05 was used for significant while ns, non-significant.
PMC9260663
fpls-13-892729-g001.jpg
0.434108
44c6c0159edb44e89b636add48a6c078
Heatmap of RNA editing efficiency of all the RNA sites in two genotypes of rice (CD, Caidao and WD, WD20342), (A) Chloroplast genome; (B) mitochondrion genome. The x-axis shows the genotypes under control (CD and WD) and treated (CDT and WDT) while the y-axis shows the editing sites. Black dotted box representing the RNA editing sites increased efficiency. (C) Reduced RNA editing efficiency in genes of mitochondria. Values insides the boxes were showing RNA editing efficiency. The x-axis shows the genotypes under control (CD and WD) and treatment (CDT and WDT). Gene names with amino acid position and type of changes were shown on the y-axis.
PMC9260663
fpls-13-892729-g002.jpg
0.426001
75c02f0627194b96995023b3bf9b587e
Gene Ontology annotation of genes of (A) chloroplast and (B) mitochondria. Red color showing cellular components (CC), blue color representing molecular functions (MF), and green color showing biological functions (BF).
PMC9260663
fpls-13-892729-g003.jpg
0.448515
4d1a060c478d4207bc3d012a071c3c1d
Expression of PPR genes (A), OZ1 genes (B), and MORF/RIP genes (C) in two genotypes of rice (CD, Caidao and WD, WD20342) under control and treatment. (D) Expression analysis of PPR, OZ1, and MORF/RIP genes through qRT-PCR in control (C) and treatment (T). Mean of three replicates with ±SE were used. For comparison t-test was used (**p < 0.01 and *p < 0.05).
PMC9260663
fpls-13-892729-g004.jpg
0.389908
1e45e587133149b296153aff429e8f76
Genome organization of Mycobacteriophage Tweety.Phage Tweety is a member of Subcluster F1, is temperate, has a siphoviral morphology (inset, electron micropraph; scale marker, 100 nm), and its genome organization illustrates several common features. The genome is represented as a bar with markers every 1 kbp, and the predicted genes are shown as colored boxes above or below the genome, indicating rightwards- and leftwards-transcription, respectively. Gene numbers are shown within the boxes and predicted functions are shown above. The virion structure and assembly genes are arranged in a rightwards-transcribed operon at the left end of the genome (genes 1 to 25), followed by the lysis cassette. The repressor (45) and putative Cro-like (46) genes are divergently transcribed, and the integration cassette (attP and 43) are located nearby, with attP defining a “left arm” from cos–attP and a “right arm” from attP–cos. Note that the left arm genes—predominantly the virion structure and lysis genes—are relatively large and have known functions, whereas the right arm genes are relatively small, and most have unknown functions. Shown are the positions of the MPME mobile element and the counterdefense gene, 54. The positions of putative early and later lytic promoters as determined by RNAseq are indicated. Note that genes are arranged in long operons such that there are relatively few transcriptional changes (tdc), such as at the 25/26 and 45/46 junctions.
PMC9262239
ppat.1010602.g001.jpg
0.416222
bbcac817d28d4378946993d541824169
Diversity of mycobacteriophage genomes displayed as network phylogenies based on shared gene content.(A) Relationships among representative members of clusters, subclusters, and singleton genomes. One member of each mycobacteriophage cluster and subcluster together with the 7 singletons were compared using Splitstree [39] with a nexus file recording the numbers of shared genes. Clusters are illustrated with colored shading; note that some clusters (e.g., Cluster A) contain several subclusters indicated as nodes, whereas other clusters are not subdivided. Singletons are shown as unlabeled black circles. (B) Diversity of Cluster F mycobacteriophages. All currently sequenced Cluster F mycobacteriophages (n = 188) are displayed as nodes in a network phylogeny using Splitstree. Colored circles show the positions of the Subclusters F2 to F5 genomes; all of the others (n = 177) are grouped in Subcluster F1. This illustrates the substantial intracluster diversity, and pairwise comparisons of Subcluster F1 phages show they may share as few as 40% of their genes.
PMC9262239
ppat.1010602.g002.jpg
0.452507
f0b4e1dc3a274d309ed94c3143a03483
Integration-dependent superinfection immunity systems.(A) Typical organization of the immunity regions of phages encoding integration-dependent immunity systems. In the viral genome, the repressor (rep) and integrase (int) genes are cotranscribed from the PRep promoter, and the phage attachment site (attP, blue box) is located within the repressor gene. The virally encoded Integrase and Repressor proteins both carry C-terminal ssrA-like tags (——LAA, or similar) targeting the proteins for proteolytic degradation (red arrows in the int and rep genes; red circles in the proteins; the N-termini are indicated). The virally encoded form of the Repressor is not active in conferring superinfection immunity. The establishment of lysogeny requires integrase-mediated site-specific recombination between the phage attP site and a chromosomal attB site (which overlaps a host tRNA gene) to form a prophage. Integrative site-specific recombination removes the ssrA-like tag from the repressor and the stable, active form of the repressor binds to the operator (OR, yellow box) to shut down the early lytic promoter (PR) and confer superinfection immunity. (B) Organization of the attP and attB sites of phage BPs and M. smegmatis. Both DNA strands are shown, and the amino acid sequence of part of the leftwards-transcribed repressor is shown; DNA and protein polarities are indicated. The 35-bp common core sequence (conserved in attP, attB, attL, and attR) is boxed, and the region within which strand exchange for recombination must occur is indicated. The codon spanning the left side of the common core is indicated by a red line, and the third position base is shown in bold pink type. The location of the tRNAarg gene at attB is shown by an arrow; the anticodon is shown in red type. (C) Organization of the BPs attL site. Conservation of the common sequence between attP and attB results in construction of an active tRNAarg gene when the prophage is established. However, at attL the repressor gene encounters a termination codon (TGA) formed at the junction of the bacterial and phage sequences, changing the third base of a cysteine codon (red line) to a nonsense codon; the third position base is shown in bold pink type. (D) Alignment of attP and attB showing the common core (boxed), and the positions of 2 mismatches in the common core, neither of which introduced mispairing in the tRNAarg product. Only the top strand of each site is shown.
PMC9262239
ppat.1010602.g003.jpg
0.465585
45252bd18a8a4a5aa4266be11a2e74d2
Chromosomal attB attachment sites used by temperate phages in M. smegmatis and M. abscessus.(A) attB sites in the M. smegmatis mc2155 genome. The 7-Mbp M. smegmatis genome is represented as a circle with markers at each kbp indicated. The attB sites (e.g., attB-1, attB-2, etc.) are shown, together with the genome coordinates in red type; the genes are shown in blue type. The font color of the M. smegmatis attB sites (i.e., attB-xsmeg) label is coordinated with homologous sites in M. abscessus (i.e., attB-xMab) shown in panel B. The names of clusters or subclusters (or the phage name if it is a singleton) within which one or more phages use that site for integration are shown in large black type. “Y” or “S” superscripts on the cluster names denote whether the site is used by tyrosine- (Y) or serine (S) -integrases. attB sites for which integration-proficient vectors have been developed are indicated with a red asterisk. (B) attB sites in the M. abscessus ATCC19977 genome mapped by identification of integrated prophages. The font color of the attB sites (i.e., attB-xMab) is coordinated with their homologues in M. smegmatis (i.e., attB-xsmeg) shown in panel A. Genome coordinates are shown in red type; genes are shown in blue type. The clusters/subclusters of prophages for which members are found integrated in those sites are shown in black type. “Y” or “S” superscripts on the cluster names denote whether the site is used by tyrosine- (Y) or serine (S) -integrases. The integration vectors based on phage L5 (attB-1smeg) integrate at a homologous site in M. abscessus (shown in box) although no prophages have been identified there. This and the attB-7Mab site are only ones for which integration vectors have been shown to work (marked with red asterisks), but several vectors developed for M. smegmatis are predicted to also work in M. abscessus (blue asterisks).
PMC9262239
ppat.1010602.g004.jpg
0.413252
0242599bd93149ccb40fff8a9563dc31
Elemental alteration in the toenails of young Saudi females with obesity.
PMC9262256
JMedLife-15-601-g001.jpg
0.503983
17c1974474164ce9a8435b7edde3a95e
(A) XRD patterns of PdAgPb@rGO/In2O3, PdPb@rGO/In2O3, PdAg@rGO/In2O3, Pd@rGO/In2O3, GO/In2O3 and In2O3, (B) diffraction peaks of Pd in PdAgPb@rGO/In2O3, PdPb@rGO/In2O3, PdAg@rGO/In2O3 and Pd@rGO/In2O3.
PMC9262407
d2ra03248a-f1.jpg
0.453598
61fe9ea7f411414cbeef5c9e7c27a91b
FE-SEM images of (A) GO/In2O3, (B) PdPbAg@rGO/In2O3, (C) HAAD-SSEM elemental mapping of Pd, Pb, Ag, In, C, O, (D) EDS of PdPbAg@rGO/In2O3.
PMC9262407
d2ra03248a-f2.jpg
0.410834
1f83584e4eb345d9a52314a9fd0ba789
(A), (B), (C) and (D) HR-TEM images of PdPbAg@rGO/In2O3 at different magnifications.
PMC9262407
d2ra03248a-f3.jpg
0.46728
85ce7d13fc5c4dc7acdf6bd1d47bdaa2
XPS spectra of (A) Survey, (B) Pd 3d, (C) Pb 4f, (D) Ag 3d, (E) C 1 s and (F) In 3d in PdPbAg@rGO/In2O3.
PMC9262407
d2ra03248a-f4.jpg
0.411419
c223b05acd214e10972c19829c1df349
CV curves of the electrocatalysts in (A) 1 M KOH and (B) 1 M KOH + 0.5 M EG (scan rate: 50 mV s−1).
PMC9262407
d2ra03248a-f5.jpg
0.409522
dd83e08b36994a619f39dff7b5c10c34
(A) EGOR curves of PdPbAg@rGO/In2O3 in 1 M KOH + 0.5 M EG solution at various scan rates. (B) curves of peak current density (jP) of four different catalysts and the square root of the scanning rate (ν1/2).
PMC9262407
d2ra03248a-f6.jpg
0.437054
ca9b40ca9876475596d1008a430fd83d
Nyquist plots of the five catalysts in (A) 1.0 M KOH + 0.5 M EG. Chronoamperometric curves of the five catalysts in (B) 1.0 M KOH + 0.5 M EG for 3600 s.
PMC9262407
d2ra03248a-f7.jpg
0.437799
4143e2e9f00f4c93997381018c7e037b
Representation of the overall flowchart of the given study.
PMC9263208
fimmu-13-836576-g001.jpg
0.439747
864b35988dc543c6b780abefa0a18e67
Genetic and expression variation of the PRG gene in HCC. (A) Comparative analysis of normal and HCC tissues based on 52 PRGs. (B) The CNV frequency of 52 PRGs in the HCC cohort. (C) Assessment of the 23 chromosomes to identify the location of CNVs among 52 PRGs in the HCC cohort. (D) Sankey diagram depicting the relationships between 52 PRGs and PR-lncRNAs (ns, no significance; *P < 0.05; **P < 0.01; ***P < 0.001).
PMC9263208
fimmu-13-836576-g002.jpg
0.413589
1daf455a472047db82a113486f366105
Establishment of the PR-lncRNA prognostic signature for HCC patients. (A) Volcano plot of differentially expressed PR-lncRNAs in HCC from entire set. (B) Venn diagram to identify differentially expressed PR-lncRNAs associated with prognosis. (C, D) Ten-fold cross-validation by the LASSO Cox regression for the prognostic value of the PR-lncRNAs in the training set. (E) The presentation of five lncRNAs in multivariate Cox regression analysis. (F) Representation of the correlations between 52 PRGs and the five prognostic PR-lncRNAs via heatmap.
PMC9263208
fimmu-13-836576-g003.jpg
0.425424
397ab968519a4c7c8fc660c927d939dd
Prognostic value of the risk model of the five PR-lncRNAs. The assessment of overall survival rate among low-risk and high-risk groups of HCC by employing Kaplan–Meier survival curves for the (A) training, (B) testing, and (C) entire set. The presentation of the level of expression of five prognostic lncRNAs via clustering analysis heatmap of each patient enrolled in (D) training, (E) testing, and (F) entire set. The coherence of survival time and survival status among the low-risk and high-risk groups and the distribution of PR-lncRNA model-based risk score for the (G) training, (H) testing, and (I) entire set.
PMC9263208
fimmu-13-836576-g004.jpg
0.458651
96f010ddc4f24202a3e6584be0885791
Assessing the accuracy and independence of the model. Curves of receiver operating characteristic (ROC) related to prognostic signature for predicting the 1, 3, and 5 years of survival in the (A) training, (B) testing, and (C) entire set. Univariate Cox regression results in the (D) training, (E) testing, and (F) entire set. Multivariate Cox regression results in the (G) training, (H) testing, and (I) entire set.
PMC9263208
fimmu-13-836576-g005.jpg
0.393873
db4d0b3ee3644900a5d4664400fb9640
Comparing the prognostic precision of the model and clinical features and comparing risk scores between subgroups with different clinical characteristics. (A–C) Prognostic accuracy of the risk scores, age, gender, grade, and tumour stage were compared using time-dependent ROC curves in the time duration of 1 year. (D–F) The concordance index was used for comparing the discrimination of the model, age, gender, grade, and tumour stage in three datasets. Risk scores are grouped by different clinical characteristics in the entire set. (G) Grade. (H) Stage. (I) Gender. (J) Age. ns, no significance; ***P < 0.001.
PMC9263208
fimmu-13-836576-g006.jpg
0.449502
55720f77ba41456cab5a07a09c05bd6b
Principal component analysis between the high-risk and low-risk groups based on (A) entire gene expression profiles, (B) 52 PRGs, (C) PR-lncRNAs, and (D) risk model based on the five PR-lncRNAs in the entire set.
PMC9263208
fimmu-13-836576-g007.jpg
0.435472
60f167f7034740e19d6848835fb418f0
Establishment and assessment of a nomogram in the entire set. (A) The nomogram predicts the probability of the 1, 3, and 5 years of OS. (B) The calibration plot prediction via nomogram of the OS at 1, 3, and 5 years. (C) ROC curves of the nomogram for predicting the 1, 3, and 5 years of survival. (D) Decision curve analysis for the nomogram, age, gender, grade, stage, and risk score. (E) C-index of the nomogram, signature, and stage.
PMC9263208
fimmu-13-836576-g008.jpg
0.437716
f752d2172c4f4e50997293dfdbff76bc
Presentation of the expression profile of immune checkpoints genes and Immune cell infiltration among low-risk and high-risk groups. (A) Barplot depicting the 22 immune infiltrating cell proportions of the high-risk and low-risk. (B) The differential proportion of the immune cells has been calculated via violin plot among low-risk and high-risk patients. (C) Boxplots depict the 29-immune signature ssGSEA scores of high-risk patients compared to low-risk patients. (D) Comparative analysis among the high- and low-risk categories on the basis of the expression profile of immune checkpoint genes (ns, no significance; *P < 0.05; **P < 0.01; ***P < 0.001).
PMC9263208
fimmu-13-836576-g009.jpg
0.464492
8a4d4ae064f64a4b8ec2b022dbc8ea76
Functional enrichment analysis, sensitivity to immunotherapy, and pyroptosis scores for the high- and low-risk groups, and external experimental validation of five PR-lncRNAs. (A) Hallmark gene set. (B) KEGG, Kyoto Encyclopedia of Genes and Genomes. (C) GO analysis. (D) TIDE score for the high- and low-risk groups. (E) Differences in pyroptosis scores between the low and high-risk groups. (F–J) The experiment confirmed the difference in the prognostic lncRNA expression between HCC and adjacent non-tumour tissues. **P < 0.01; ***P < 0.001.
PMC9263208
fimmu-13-836576-g010.jpg
0.458657
6b14f2b2cfa647b0905ec1a710120bab
The assignment of edge (solid lines) for macaques’ human co-interaction networks, based on their co-occurrence and joint interactions with humans (dotted lines) within the same time (10-min time-frames) and space (pre-defined blocks of anthropogenic features within the macaques’ home-ranges) (more details in43).
PMC9263808
41598_2022_15713_Fig1_HTML.jpg
0.471624
45897e2bc29845c8b9690c03b6780d93
A typical Susceptible-Infected-Recovered (SIR) model simulation of network-mediated disease transmission.
PMC9263808
41598_2022_15713_Fig2_HTML.jpg
0.461235
3fa54c9018a14a688e7bd3bb44ce926e
Scatterplots showing positive correlations, and the differences in these correlations (slopes) across contexts, between the strength centrality of first-infected macaques through their human co-interaction networks and their grooming networks, for each host species.
PMC9263808
41598_2022_15713_Fig3_HTML.jpg
0.500075
d7f0d30835734ab992c91d4f23fe4897
Plots of standardized model-coefficients (Y-axis; values from Table 2) to show the effects of the strength centrality of first-infected macaques on outbreak sizes by species, through co-interaction networks and grooming networks. Error bars represent 95% confidence intervals for each coefficient.
PMC9263808
41598_2022_15713_Fig4_HTML.jpg
0.485646
9200da3331034ac2bae3e3a8ce2f4087
An illustration of the variational autoencoder architecture for one input data modality.
PMC9264122
formative_v6i6e36998_fig1.jpg
0.44643
e1fb31a715104be397bc8235fd24fdfe
Deep representation learning for pain prediction (A: data analysis, B: deep representation learning, and C: predictive modeling).
PMC9264122
formative_v6i6e36998_fig2.jpg
0.418398
87963a00753345489a7170188a9e53d1
Visualization of the learned data representations using t-SNE: t-distributed stochastic neighboring embedding projections. VAE: variational autoencoder.
PMC9264122
formative_v6i6e36998_fig3.jpg
0.479252
6ed2c40f65b5475f9002c49f1ac6cec6
Confusion matrix for the best-performing model with original data representations for 2 pain score levels (pain scores: no or mild=0-5 and severe=6-10; Table 2, model b).
PMC9264122
formative_v6i6e36998_fig4.jpg
0.476691
094ab6f913a5460e94b2dc4ad6f99a2e
Confusion matrix for the best-performing model with variational autoencoder data representations for 2 pain score levels (pain scores: no or mild=0-5 and severe=6-10; Table 2, model e).
PMC9264122
formative_v6i6e36998_fig5.jpg
0.431639
d5f48ee1f14a468da110c95a66f7e38d
Confusion matrix for the best-performing model with original data representations for 4 pain score levels (pain scores: none=0, mild=1-3, moderate=4-6, and severe=7-10; Table 2, model a).
PMC9264122
formative_v6i6e36998_fig6.jpg
0.453527
556406b4646148cc987a1aafd0bad77f
Confusion matrix for the best-performing model with variational autoencoder data representations for 4 pain score levels (pain scores: none=0, mild=1-3, moderate=4-6, and severe=7-10; Table 2, model d).
PMC9264122
formative_v6i6e36998_fig7.jpg
0.427744
880f9517e9f44fd8a433ca108be260e1
Distribution of medication dosage with pain score for sample patients with high and moderate mean pain intensity.
PMC9264122
formative_v6i6e36998_fig8.jpg
0.434491
6e39a0e4ab0045a1991e30827d774c17
Initial presentation and the cumulative risk of pneumothorax in LAM. A Initial chief complaint of LAM patients. Ninety-eight (24.5%) patients had pneumothorax as the first symptom of LAM. Skin lesions refer to skin manifestations in patients with TSC-LAM. B In situations where pneumothorax was not the initial symptom of LAM, the cumulative risk of pneumothorax at 5, 10, and 20 years after the initial symptom was 12.5%, 22.5%, and 42.7%, respectively
PMC9264575
13023_2022_2418_Fig1_HTML.jpg
0.421132
a952b839aeb3447da596dfba409d6521
Effects of sirolimus on pneumothorax recurrence. A Definition of the sirolimus group (treated period) and control group (untreated period) in the historical prospective self-controlled study. Patients started in the control group, and once they started taking sirolimus, they were transferred to the sirolimus group for continued observation. B Kaplan–Meier analysis for the self-controlled study. The 5-year probability of pneumothorax recurrence was 80% lower in the sirolimus group than in the control group (P < 0.001 by log-rank test). C Kaplan–Meier analysis of LAM patients, removing the influence of pleurodesis. The 5-year risk of pneumothorax recurrence remained lower in the sirolimus group than in the control group (P < 0.001 by log-rank test). D Comparison of the recurrence interval between the first and the second pneumothorax and between the second and third pneumothorax in LAM patients
PMC9264575
13023_2022_2418_Fig2_HTML.jpg
0.505767
58a734e784e0418b9485908a7612c565
Concordance analyses by determination of Cohen’s kappa coefficients. Prevalence of the eight most frequent HR HPV (high risk human papilloma virus) types and comparison between the different anatomical areas. κ = 0.01–0.20 (slight concordance); κ = 0.21–0.40 (fair concordance); κ = 0.41–0.60 (moderate concordance); κ = 0.61–0.80 (substantial concordance); κ = 0.81–1.00 ((almost) perfect concordance).
PMC9264762
cancers-14-03136-g001.jpg
0.480374
dc61c386aa764b5da487b42db72d147c
HPV distribution by age group. HPV = human papilloma virus.
PMC9264762
cancers-14-03136-g002.jpg
0.440785
0c49f8eedc0043e0971be330a4eccf1c
Incidence of distribution for wooden breast (WB) and spaghetti meat (SM).
PMC9264991
animals-12-01617-g001.jpg
0.446612
1ad8ddd3ecfc403dbbf787cea761840e
Occurrence of delirium for different surgical procedures concerning fluid intake. A total of 18.2% of the patients in group A and 48% of the patients in group B develop delirium. (Group A: reconstruction with primary wound closure or local flap. Group B: microsurgical reconstruction with free flap).
PMC9265071
cancers-14-03176-g001.jpg
0.449439
ff9342b43c03407f94ef77e52abdb139
Chest computed tomography (CT). (A) Chest CT on admission demonstrating probably dependent atelectasis of the basal aspect of the right lower lobe and (B) on day 6 after admission indicating new-onset extensive consolidation and ground-glass opacity of the right middle lobe, lingular segment, and both lower lobes with increased right pleural effusion.
PMC9265713
ijerph-19-07954-g001.jpg
0.417547
8d40309286a245b3bdf18f3cbf5babbc
Changes in plain chest radiography (PA) with the clinical course. (A) No active disease at the time of admission. (B) Deterioration during hospitalization (6 days after admission); pneumonia or pulmonary edema; bilateral pleural effusion or thickening. (C) Improvement in pulmonary edema 13 days after admission. (D) No active disease at the time of outpatient follow-up (7 days after discharge).
PMC9265713
ijerph-19-07954-g002.jpg
0.45596
634d1e87c5cb4993b6ca9f372a73af7b
Clinical appearance of squamous bulbar conjunctival lesions including a lobulated papilloma extending toward the inferior fornix from Case 3 (A), a more nodular CIN encroaching on the limbus from Case 39 (B), and a larger invasive perilimbal SCC with prominent conjunctival hyperemia from Case 51 (C). Representative low-magnification histology of conjunctival lesions including a papilloma characterized by hyperplastic epithelium overlying fibrovascular core denoted with asterisks (D) (scale bar: 100 μM), a CIN exhibiting a thickened and dysplastic epithelium (asterisks) (E) (scale bar: 50 μM), and an invasive SCC with neoplastic cells breaching the epithelial basement membrane and infiltrating the substantia propria (asterisk) (F) (scale bar: 100 μM). Higher magnification of a representative conjunctival papilloma with large numbers of PAS-positive goblet cells (arrows) and infiltrating neutrophils (G) (scale bar: 25 μM), CIN with abnormal epithelial stratification and hyperchromatic and pleomorphic nuclei (arrows) (H) (scale bar: 25 μM), and invasive SCC with epithelial dysplasia (asterisks) and intervening inflamed stroma (I) (scale bar: 25 μM).
PMC9266440
ijms-23-07249-g001.jpg
0.445113
13aa84a3122c4f4cba6a53d348957526
Representative images of in-situ hybridization showing diffuse low-risk HPV positivity in a papilloma from Case 6 using RNA probes (A) (scale bar: 100 μM). At higher magnification, many nuclei are almost completely filled with smaller dot-like foci of staining (arrows) (B) (scale bar: 25 μM). More focal high-risk HPV positivity in a papilloma from Case 16 using DNA probes (C) (scale bar: 25 μM).
PMC9266440
ijms-23-07249-g002.jpg
0.472819
d8566f490d73496984e58620d90ee8b1
Representative images from the periphery of an H&E-stained CIN from Case 39 showing the transition to non-neoplastic conjunctiva (A) (scale bar: 25 μM). Increased nuclear immunolabeling for Ki67 within the neoplastic epithelium (B) and corresponding RNA in-situ hybridization demonstrating positivity for high-risk HPV within the same dysplastic cells (C). Arrows in A–C mark the border between CIN and adjacent conjunctiva with non-dysplastic epithelium on the right side of each panel negative for Ki67 and HPV. The underlying substantia propria, containing blood vessels and inflammatory cells, is marked by asterisks and is negative for HPV. Representative images of an H&E-stained CIN from Case 40 (D) (scale bar: 25 μM) and cCIS from Case 44 (G) (scale bar: 25 μM) with arrows pointing to the epithelial base and asterisks in the underlying substantia propria. Increased nuclear immunolabeling for Ki67 within the neoplastic epithelium (E,H) and the corresponding RNA in-situ hybridization, which were both negative for high-risk HPV (F,I).
PMC9266440
ijms-23-07249-g003.jpg
0.427505
5f2155c8ca744c389606f78c8e56f12a
H&E-stained section of Case 1, a conjunctival papilloma demonstrating reactive epithelial atypia associated with inflammation (A) (scale bar: 50 μM). Reactive atypia and mixed inflammation characterized by neutrophils (arrows) and fewer lymphocytes and plasma cells within the epithelium from Case 1 at higher magnification (B) (scale bar: 25 μM). HPV in Case 1 was confirmed with RNA in-situ hybridization, with diffuse LR HPV in (C) (scale bar: 50 μM) and shown at higher magnification with dot-like foci of signal, some of which coalesced into larger masses (arrows) (D) (scale bar: 25 μM). HR HPV was not detected in these same epithelial cells (E) (scale bar: 25 μM). Diffuse koilocytosis (arrows) in the well-differentiated epithelium of a recurrent LR HPV-positive papilloma from Case 14 (F) (scale bar: 25 μM).
PMC9266440
ijms-23-07249-g004.jpg
0.408947
18cc2aecc4424022a820da62811fd0ec
IH-induced increases in transendothelium passage of LDL and monocytes in vitro are prevented by inhibitors of VE-cadherin cleavage. (a) Inhibiting HIF-1 by acriflavine, Src-kinases by saracatinib and VEGF receptor tyrosine kinases by pazopanib, prevented the IH-induced increase in transendothelium passage of LDL (2-way ANOVA, ** p < 0.01 vs. N + DMSO, n= 28 for DMSO, n = 8–12). (b) Inhibiting HIF-1 by acriflavine, Src-kinases by saracatinib and VEGF receptor tyrosine kinases by pazopanib prevented the IH-induced transendothelium migration of monocytes (2-way ANOVA, * p < 0.05 and *** p < 0.001 vs. N + DMSO, # p < 0.05 and ## p < 0.01 vs. IH + DMSO, n = 10–11). Values are mean ± SEM. Control experiments: DMSO (vehicle of the inhibitors). N: normoxia, IH: intermittent hypoxia.
PMC9266969
ijms-23-07012-g001.jpg
0.490842
a7f1be22880f48e09bc071c6c1905a8c
Intermittent hypoxia impairs VE-cadherin integrity in vivo in C57BL/6J mice, which is prevented by inhibitors of VE-cadherin cleavage. (a) IH increased sVE level in the plasma of C57BL/6J mice treated with vehicle (DMSO) after 14 days of exposure to IH, semi-quantitatively measured by Western blotting (N vs. IH at day 14, ** p < 0.01, Welch t-test, n = 21–22, values are mean ± SEM). (b) A representative example of Western blot showing a more intense sVE-band in the plasma of mice exposed to IH compared to those exposed to normoxia for 14 days (the immunoglobulin band is used as a loading control for normalization). (c) A representative example showing a more intense VE-cadherin fluorescence on the endothelium in N not in IH. Arrows indicate the VE-cadherin fluorescence in green in the endothelium, and the blue staining corresponds to nuclei stained with DAPI. (d) IH reduced VE-cadherin expression in the endothelium of C57BL/6J mice after 14 days of exposure to IH (N vs. IH at day 14, *** p < 0.001, Welch t-test, n = 15–16, values are mean ± SEM). (e) Inhibiting HIF-1 (by ACF) prevented the IH-induced elevation of sVE level in the plasma of C57BL/6J mice exposed for 14 days to IH or N (Kruskal-Wallis test, * p < 0.05 vs. N + vehicle, ## p < 0.01 vs. IH + vehicle, n = 6–8, values are median + interquartile range). (f) Inhibiting VEGFR tyr-kinases (by pazopanib) or src-kinases (by saracatinib) prevented the IH-induced elevation of sVE level in the plasma of C57BL/6J mice exposed for 14 days to IH or N (Kruskal-Wallis test, * p < 0.05 and ** p < 0.01 vs. N + vehicle, ## p < 0.01 vs. IH + vehicle, n = 5–8, values are median + interquartile range). N: normoxia, IH: intermittent hypoxia.
PMC9266969
ijms-23-07012-g002.jpg
0.482309
7e5c26c7449941d79f44617ab3634cf3
The effect of the inhibition of VE-cadherin cleavage pathways on intima-media thickness in C57BL/6J mice. (a) Representative images of aortic cross-sections stained with Hematoxylin-Eosin. (b) Inhibiting HIF-1 (by ACF) prevented the IH-induced elevation of IMT in C57BL/6J mice exposed to IH for 14 days, compared to N (Kruskal-Wallis test, ** p < 0.01 vs. N + vehicle, ### p < 0.001 vs. IH + vehicle, n = 7–8). (c) Inhibiting VEGFR tyr-kinases (by pazopanib) and src-kinases (by saracatinib) prevented the IH-induced elevation of IMT in C57BL/6J mice exposed 14 days to IH, compared to N (Kruskal-Wallis test, ** p < 0.01 vs. N + vehicle, # p < 0.05 vs. IH + vehicle, n = 5–8). (N: normoxia, IH: intermittent hypoxia. Values are median + Interquartile range. Scale bars = 50 µm.
PMC9266969
ijms-23-07012-g003.jpg
0.505477
b946589fe6864822a59910ce0fe1a84b
The effect of the inhibition of VE-cadherin cleavage pathways on aortic elastic lamellae in C57BL/6J mice. (a) Representative images of Weigert-stained aorta cross-sections (red arrows indicate elastic lamella disruptions). (b) Inhibiting HIF-1 (by ACF) prevented the elevation of elastic lamella disruptions induced by IH (Kruskal-Wallis test, * p < 0.05 vs. N + vehicle, n = 7–8). (c) Inhibiting src-kinases (by saracatinib) prevented the elevation of elastic lamella disruptions induced by IH. Inhibiting VEGF receptor tyrosine kinases (by pazopanib) had no effect on the elevation of elastic lamella disruptions induced by IH (Kruskal-Wallis test, *** p < 0.001 vs. N + vehicle, # p < 0.05 vs. IH + vehicle, & p < 0.05 N + Pazopanib vs. IH + Pazopanib, n = 5–8). (d) Inhibiting HIF-1 (by ACF) prevented the IH-induced thinning of elastic lamellae (Kruskal-Wallis test, * p ≤ 0.05 vs. N + vehicle, n = 5). (e) Inhibiting src-kinases (by saracatinib) prevented the IH-induced thinning of elastic lamellae. Inhibiting VEGF receptor tyrosine kinases (by pazopanib) had no effect on the IH-induced thinning of elastic lamellae (Kruskal-Wallis test, * p ≤ 0.05 vs. N + vehicle, & p < 0.05 N + Pazopanib vs. IH + Pazopanib, n = 5). N: normoxia, IH: intermittent hypoxia. Mice were exposed to N or IH for 14 days. Values are median + Interquartile range. Scale bar = 50 µm.
PMC9266969
ijms-23-07012-g004a.jpg
0.461692
e787db72274647e58354de7c01baf2e6
The impact of the inhibition of VE-cadherin cleavage pathways on atherosclerosis lesions in ApoE-/- mouse aortas. (a) Representative examples of ORO-stained entire aortas. (b) Inhibiting HIF-1 (by ACF) prevented atherosclerotic plaques in aortas of ApoE-/- mice exposed for 8 weeks to IH (Kruskal-Wallis test, ** p < 0.01 vs. N + vehicle, n = 5–8). (c) Inhibition of VEGFR tyr-kinases (by pazopanib) and src-kinases (by saracatinib) prevented the formation of atherosclerotic plaques in aortas of ApoE-/- mice exposed for 8 weeks to IH (Kruskal-Wallis test, * p < 0.05 vs. N + vehicle, ## p < 0.01 vs. IH + vehicle, n = 5–6). (d) Inhibiting HIF-1 (by ACF) tended to reduce atherosclerotic plaques in aortic roots of ApoE-/- mice exposed for 8 weeks to IH (Kruskal-Wallis test, p = 0.08 for N + vehicle vs. IH + vehicle, n = 4–8). (e) Inhibition of VEGFR tyr-kinases (by pazopanib) and src-kinases (by saracatinib) reduced the atherosclerotic plaque area in aortic roots of ApoE-/- mice exposed for 8 weeks to IH (Kruskal-Wallis test, # p < 0.05 vs. IH + vehicle, n = 5–6). N: normoxia, IH: intermittent hypoxia. Values are median + interquartile range.
PMC9266969
ijms-23-07012-g005.jpg
0.43401
b5b63111de1f492f86d9d586b5bb4dee
The impact of blocking VE-cadherin cleavage pathways on arterial blood pressures of ApoE-/- mice. (a) Inhibiting VEGFR tyr-kinases (by pazopanib) and src-kinases (by saracatinib) prevented the hypertensive effect of IH on arterial blood pressures in ApoE-/- mice exposed to IH for 8 weeks (3-way ANOVA, followed by a Fisher’s LSD test, * p < 0.05 vs. N + vehicle, # p < 0.05 vs. IH + vehicle, n = 5–8). (b) IH induced a trend towards elevation of blood pressure, and acriflavine tended to reduce this effect in ApoE-/- mice exposed to IH for 8 weeks (3-way ANOVA, p = 0.17 for the interaction IH × treatment, n = 5–8). Values are mean ± SEM. N: normoxia, IH: intermittent hypoxia. veh: vehicle. SBP = systolic blood pressure, DBP = diastolic blood pressure, MAP =mean blood pressure.
PMC9266969
ijms-23-07012-g006.jpg
0.418166
6a4047335b3f47babc1062c19bbca91e
Effect of the various treatment solutions on Streptococcus mutans biofilm formation: saline as negative control; herbal extracts (HE); combined herbal extracts and hydroxyethyl cellulose (HE + HEC); and chlorhexidine (CHX) as positive control. Results (±standard deviation) are presented as absorbance at 600 nm.
PMC9267188
materials-15-04652-g001.jpg
0.44589
8bbbdb463a67414798d92f03037665e2
Effect of the various treatment solutions on Streptococcus mutans lactic acid production: saline as negative control; herbal extracts (HE); combined herbal extracts and hydroxyethyl cellulose (HE + HEC); and chlorhexidine (CHX) as positive control. Results (±standard deviation) measured using a colorimetric assay are presented as OD (600 nm) units.
PMC9267188
materials-15-04652-g002.jpg
0.511498
796223f56ed444c39647dbdfbf1eb76e
Effect of the various treatment solutions on Streptococcus mutans ATPase activity: saline as negative control; herbal extracts (HE); combined herbal extracts and hydroxyethyl cellulose (HE + HEC); and chlorhexidine (CHX) as positive control. Results (±standard deviation) measured using a colorimetric assay are presented as OD (600 nm) units.
PMC9267188
materials-15-04652-g003.jpg
0.415252
c7087357e2f4428486a80b7f6054da8c
Fluorescent microscopy images showing EPS production (maroon-stained indicated by arrow) in the biofilms of the various treated samples: (a) saline; (b) herbal extracts; (c) combined herbal extracts and hydroxyethyl cellulose; and (d) chlorhexidine.
PMC9267188
materials-15-04652-g004a.jpg
0.483641
d69e0ca7e1b74bdf97e0b40741d36b55
Effect of the various treatment solutions on Streptococcus mutans EPS production: saline as negative control; herbal extracts (HE); combined herbal extracts and hydroxyethyl cellulose (HE + HEC); and chlorhexidine (CHX) as positive control. Results (±standard deviation) are presented as percentage of maroon-stained pixels measured from digitally analyzed (Image J, NIH) fluorescent microscopy images.
PMC9267188
materials-15-04652-g005.jpg
0.448621
2f1d9bf03f0e42f09bd64add6f5c70aa
General concept of model.
PMC9267376
materials-15-04440-g001.jpg
0.428866
289e3e3d451d43c0b5c84ff37ff28425
Model supporting stabilization quality of industrial products.
PMC9267376
materials-15-04440-g002.jpg
0.441683
6398f68032a447d0a0c353723c1901f1
Crack on the outer hull of four-point bearing.
PMC9267376
materials-15-04440-g003.jpg
0.467533
9139ea728d554a03b83f8e986a2bddb1
Ishikawa diagram for a crack in the bearing housing.
PMC9267376
materials-15-04440-g004.jpg
0.482178
f0c9d504ab8c4f6c99768276e862176e
Ishikawa diagram for crack on the outer hull of four-point bearing to assess the importance of potential causes.
PMC9267376
materials-15-04440-g005.jpg
0.473416
7df7f01f52d64924b0b38a303938e378
Ishikawa diagram for crack on the outer hull of four-point bearing to choose the second-order causes.
PMC9267376
materials-15-04440-g006.jpg
0.446134
77866747aeb14cd8b4439c158067938a
Ishikawa diagram for crack on the outer hull of four-point bearing to choose the main cause.
PMC9267376
materials-15-04440-g007.jpg
0.441381
42528e865f9d4bc48e843f5b0488c4a6
mRNA degradation mechanisms through ASO and siRNA. (A) The ASO mechanism of action: The single-strand ASO enters the cell and the nucleus; once it is bound to the mRNA, the double-strand siRNA is recognized by RNAse H and degraded. (B) The siRNA mechanism of action: The double-strand siRNA enters the cell; in the cytoplasm, the duplex opens and the antisense strand binds to the RNA-induced silencing complex (RISC). The mRNA is recognized by the antisense-RISC complex and degraded.
PMC9267663
jcm-11-03884-g001.jpg
0.534113
ffb9f17d577f40e2be8e3faea525f3b2
Different ASO generations.
PMC9267663
jcm-11-03884-g002.jpg
0.447047
5c8f62485c594a369f4b1d992219d81f
Kaplan–Meier survival curve between HF patients with and without COPD.
PMC9267665
jcm-11-03709-g001.jpg
0.446894
f20d9c1ba49948f39efcd445ae108030
The process of sieving and separating parts of hemp. Material A: whole dried hemp; B: dried seedless and wasteless hemp; C: hemp powder - the first half of the sifted material in a sieve (3); D: hemp powder - the other half of the sifted material in a sieve (3); E: material residue on sieve (3); F: material remaining in the sieve (2); G: pure hemp seeds and H: waste material (mainly stems).
PMC9269414
plants-11-01749-g001.jpg